Lung surfactant-derived fatty acids are a primary carbon source for the opportunistic human pathogen, Pseudomonas aeruginosa (PA), in the airways of people with cystic fibrosis. However, the mechanisms underlying the breakdown of these fatty acids by PA, as well as the potential implications of fatty acid degradation on the virulence, remain incompletely elucidated. Here, we compared the proteomes of a Manchester epidemic strain Pa10348 growing on octanoate (C8:0), palmitate (C16:0) and oleate (C18:1) with the proteome of that growing on commonly explored carbon source, glucose.